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To the Editor:-We have been very interested by the recent report of 11 cardiac transplantation recipients who underwent elective laparoscopic cholecystectomy. [1 ] This report is a useful adjunct to our knowledge on pneumoperitoneum-induced hemodynamic changes because previous series have reported that cholecystectomy is well tolerated in these patients, but they did not offer any detailed hemodynamic information. We were concerned by the use of a pulmonary artery catheter because these patients are immunosuppressed and also because pneumoperitoneum may impair venous return, which is critical to hemodynamic tolerance in patients with a transplanted heart. Pulmonary artery occlusion pressure and central venous pressure increased, but the authors could only speculate on the origin of this change because pleural pressure was not measured. We describe the use of transesophageal echocardiography to monitor hemodynamic changes induced by laparoscopic for cholecystectomy in a patient with transplanted heart.

A 26-yr-old man was scheduled for a laparoscopic cholecystectomy due to recurrent episodes of biliary colic. He had undergone an orthotopic cardiac transplantation 8 months previously. His physical examination demonstrated a systolic murmur and a mild hypertension at 150/100 mmHg, treated with diltiazem. Immunosuppression was maintained with methylprednisolone, azathioprine, and cyclosporine. Transthoracic echocardiography showed a normal left ventricular systolic function and no valvular abnormality. An exercise test was performed on a cycle ergometer to evaluate heart changes during a physical effort. Loading was increased by 30 W every 3 min until the patient could no longer pedal at 60 rpm. Cardiac responses were typical of a denervated heart. [2 ] Heart rate was high at rest (98 beats/min), although changes occurred slowly and began only after 3 min of exercise. Peak exercise heart rate was low (129 beats/min). Exercise test was terminated at 120 W because of leg fatigue.

Before induction of anesthesia, electrocardiograph with ST segment analysis and pulse oximetry were monitored. Blood pressure was measured noninvasively. Anesthesia was induced with 300 mg of thiopental and 25 micro gram of sufentanil. Endotracheal intubation was facilitated by 50 mg of atracurium. Anesthesia was maintained with sufentanil, desflurane, and nitrous oxide in oxygen (inspired oxygen, 50%). The patient also was monitored for neuromuscular blockade, desflurane, and CO sub 2 end-tidal concentrations and esophageal temperature. Additionally, a transesophageal echocardiographic probe (TEE) was inserted immediately after induction, and hemodynamic calculations were made according to a previous report. [3 ]

After induction of anesthesia, mean arterial pressure (MAP) and heart rate (HR) decreased moderately (Table 1). The first cardiac output (CO) measurement was 5.1 l/min. After peritoneal insufflation, MAP, HR, and CO increased. Deepening anesthesia with increasing concentrations of desflurane led to partial correction of the increased MAP. After exsufflation, MAP and CO returned to prepneumoperitoneum values.

In our patient, CO slightly increased after insufflation, whereas left ventricular preload (estimated by end diastolic area) remained unaltered. Most recent studies have shown, contrary to older reports, [4 ] that CO and preload are maintained (or even increased) after peritoneal insufflation. These data have been obtained using either invasive methods (radial artery pressure profile, [5 ] pulmonary artery catheter, [6 ]) or TEE [7,8 ] in healthy patients. Preservation or even increase in CO also was observed in ASA physical status 3 patients. [9 ] These authors speculated that surgery-induced sympathetic stimulation was the main cause, [9 ] but increase in preload by increase in venous return from the lower part of the body also may be possible. [8 ] As previously suggested, [1,9 ] hemodynamic tolerance is improved when pneumoperitoneum is created in patients in the supine position.

The resting HR of our patient was elevated (92 beats/min), reflecting parasympathetic denervation. [2,10 ] HR decreased after induction of anesthesia and then increased during CO2insufflation. Many authors have also found this small increase in HR, but the change is usually not significant. [4,7 ] This increase in HR suggests a reflex sympathetic cardiac response, whereas the immediate increase in MAP suggests a sympathetic response on peripheral vessels. The exercise test highly suggests that our patient's heart had not undergone sympathetic reinnervation. In the denervated transplanted heart, the increase in HR is delayed and depends on catecholamines. [10 ] It is thus possible that the increase in HR can be explained by an increase in catecholamines, resulting from incisional pain 3 min before CO2insufflation. Administration of increasing concentrations of desflurane also may have led to catecholamine release and HR and MAP increases.

This case report supports the belief that, in a heart-transplanted patient with normal left ventricular function, pneumoperitoneum is hemodynamically well tolerated.